While conflicting reports exist [31, 32], in a mouse model of hereditary hemochromatosis, changes in cardiac ABCB8 expression were reported to regulate DOX retention and cardiotoxicity, with decreased ABCB8 corresponding to DOX retention and ABCB8 overexpression corresponding with DOX efflux [31]. This evidence concerns the gene ABCB8 and hereditary hemochromatosis.